Autoimmune and inflammatory responses in Kashin-Beck disease compared with rheumatoid arthritis and osteoarthritis.

To examine plasma levels of arthritis-related autoantibodies and inflammatory factors in Kashin-Beck disease (KBD) patients compared with rheumatoid arthritis (RA) patients, osteoarthritis (OA) patients, and healthy controls, the plasma levels of autoantibodies to types II, IX, and XI collagen and cyclic citrullinated peptide (CCP) and immunoglobulin (Ig)-G and IgM rheumatoid factors (IgG-RF and IgM-RF) from 45 KBD patients, 39 RA patients, 46 OA patients, and 30 healthy controls were determined by enzyme-linked immunosorbent assay. The plasma concentrations of nitric oxide (NO) and tumor necrosis factor-α (TNF-α) were measured using the Griess method and bioassay, respectively. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference t test for differences among groups. Results indicated that the plasma levels of collagen IX antibodies, IgG-RF, and NO significantly increased in KBD patients compared with patients with RA and OA and the control group. The levels of collagen XI antibodies, CCP antibodies, and IgM-RF but not collagen II antibodies and TNF-α were significantly increased in the plasma of the KBD group compared with that of the control group. We conclude that autoimmunity and inflammation may be involved in the pathogenesis of KBD, in particular in the advanced stage.

NF-kappaB binding activity and pro-inflammatory cytokines expression correlate with body mass index but not glycosylated hemoglobin in Chinese population.

AIMS: Chronic inflammation is linked to type 2 diabetes (T2DM), so we investigated correlations between obesity, blood glucose levels, and inflammation in T2DM patients. METHODS: Peripheral blood mononuclear cells (PBMCs) were collected from 40 T2DM patients (27 men, 13 women; mean age 49.63 years), and 10 non-diabetic controls (all men; mean age 38.60 years). Inflammation was measured as DNA-binding activity of nuclear factor kappaB (NF-kappaB), a key transcription factor in inflammation. Protein levels of NF-kappaB subunit p65, and NF-kappaB inhibitor IkappaBalpha were assessed by Western blot. Transcript levels for p65, IkappaBalpha, and the NF-kappaB target genes TNF-alpha, MMP-9, IL-6, IL-8, and IL-18 were measured by real-time PCR. Body mass index (BMI) and glycohemoglobin were measured for all the subjects. RESULTS: NF-kappaB DNA-binding activity, p65 and IkappaBalpha protein levels, and expression of IL-6, TNFalpha and MMP-9 were significantly higher in PBMCs from T2DM patients, than from non-diabetic controls. NF-kappaB binding was significantly positively associated with both BMI and homeostasis model assessment of insulin resistance (HOMA-IR). CONCLUSIONS: Inflammation was observed in PBMCs in T2DM patients in a Chinese population, and correlated independently with obesity and blood glucose levels. Lack of correlation with glycohemoglobin suggested that moderate-term blood glucose control did not mitigate inflammation.